中药赤芍对球囊损伤术后血管重构的干预研究

目的 观察中药赤芍防止球囊损伤术后血管重构作用。方法 新西兰白兔随机分为对照组、单纯高脂组、赤芍高剂量组、低剂量组。高脂喂养6周建立动脉粥样硬化模型,行颈动脉球囊损伤术,8周时取材作病理形态学检查。结果(1)与高脂组比较,赤芍高、低剂量组增生内膜面积、中层面积,内膜、中膜、外膜PCNA阳性着色均显著减少(P<0.05或P<0.01)。(2)各组内皮增生成分主要为平滑肌细胞;巨噬细胞阳性着色主要分布在外膜,与高脂组比较,赤芍高、低剂量组阳性着色较少。(3)高脂组动脉损伤侧外膜Ⅰ型胶原增多,赤芍组Ⅰ型胶原增加较少。结论 赤芍对高脂喂养兔颈动脉球囊损伤术后血管重构有显著防止作用。     

Activation and Migration of Adventitial Fibroblasts Contributes to Vascular Remodeling

The rat carotid artery balloon injury model was used to prove the activation and migration of adventitial fibroblasts. We found that at day 7 after injury, adventitial fibroblasts proliferated, transformed into myofibroblasts under transmission electron microscopy in the model group. Simultaneously, we proved that the adventitial cells migrated to the media and intima on seventh day after injury by directly labeled the adventitial cells by the in vivo gene transfer technique. Moreover, we captured the precise moment when the adventitial fibroblasts migrated from the adventitia to the media through the external elastic plate under transmission electron microscope. This study provides direct evidences that adventitial fibroblasts activate and migrate to the media and intima, then actively take part in revascularization. Anat Rec, 301:1216–1223, 2018. © 2018 Wiley Periodicals, Inc.     

雌激素对血流动力学及多发性大动脉炎血管重构的影响

以多发性大动脉炎模型做试验,观察大动脉空间几何形态重构。测定血浆雌激素、孕激素和一氧化氮产物（NO     

安体舒通对糖尿病大鼠血管生成素1和血管生成素2表达的影响

目的观察安体舒通对1型糖尿病大鼠肾皮质血管生成素-1(Ang-1)、血管生成素-2(Ang-2)及肾脏血管重建的影响,并初步探讨其机制。方法建立1型糖尿病大鼠模型,用安体舒通干预8周后观察大鼠肾脏血管重建改变,用放射免疫法测定大鼠血浆及肾组织醛固酮水平,用RT-PCR检测各组肾皮质Ang-1和Ang-2mRNA表达。观察安体舒通对上述指标的影响。结果与糖尿病组相比,安体舒通组大鼠肾血管重建改善,血浆及肾组织醛固酮水平更高,Ang-1和Ang-2mRNA表达减少。结论安体舒通通过拮抗醛固酮的作用,减少Ang-1和Ang-2mRNA表达,改善糖尿病肾血管重建从而发挥肾脏保护作用。     

Cytomegalovirus Impairs Cytotrophoblast-Induced Lymphangiogenesis and Vascular Remodeling in an in Vivo Human Placentation Model

We investigated human cytomegalovirus pathogenesis by comparing infection with the low-passage, endotheliotropic strain VR1814 and the attenuated laboratory strain AD169 in human placental villi as explants in vitro and xenografts transplanted into kidney capsules of SCID mice (ie, mice with severe combined immunodeficiency). In this in vivo human placentation model, human cytotrophoblasts invade the renal parenchyma, remodel resident arteries, and induce a robust lymphangiogenic response. VR1814 replicated in villous and cell column cytotrophoblasts and reduced formation of anchoring villi in vitro. In xenografts, infected cytotrophoblasts had a severely diminished capacity to invade and remodel resident arteries. Infiltrating lymphatic endothelial cells proliferated, aggregated, and failed to form lymphatic vessels. In contrast, AD169 grew poorly in cytotrophoblasts in explants, and anchoring villi formed normally in vitro. Likewise, viral replication was impaired in xenografts, and cytotrophoblasts retained invasive capacity, but some partially remodeled blood vessels incorporated lymphatic endothelial cells and were permeable to blood. The expression of both vascular endothelial growth factor (VEGF)-C and basic fibroblast growth factor increased in VR1814-infected explants, whereas VEGF-A and soluble VEGF receptor-3 increased in those infected with AD169. Our results suggest that viral replication and paracrine factors could undermine vascular remodeling and cytotrophoblast-induced lymphangiogenesis, contributing to bleeding, hypoxia, and edema in pregnancies complicated by congenital human cytomegalovirus infection.Human cytomegalovirus (HCMV) is the leading cause of congenital viral infection, with an incidence in the United States of approximately 1% to 3% of live births.¹ Primary maternal HCMV infection during gestation poses a 40% to 50% risk of intrauterine transmission, whereas recurrent infection in seropositive mothers rarely causes disease.^2,3 Symptomatic infants (25%) have intrauterine growth restriction (IUGR) and permanent birth defects, including neurological deficiencies, retinopathy, and sensorineuronal deafness.^4–6 Congenital disease is more severe when primary maternal infection occurs in the first trimester.⁷ IUGR and spontaneous abortion in the absence of fetal HCMV infection can result from placental pathology.^8–10 Placentas infected in early gestation show long-standing damage and fibrosis at the uterine-placental interface, which impairs critical functions and results in a hypoxic intrauterine environment.^10–15 Despite the prevalence and the medical and societal impact of congenital HCMV infection, the mechanisms of virus replication, pathogenesis, and transplacental transmission are still unresolved because of the complex nature of placental development and extreme species specificity of HCMV, which replicates only in human tissues.Differentiating/invading cytotrophoblasts switch to an endothelial phenotype in a process that is similar to vasculogenesis.¹⁶ The cells up-regulate novel adhesion molecules and proteinases that enable their attachment to and invasion of the uterus. Interstitial invasion requires down-regulation of integrins characteristic of epithelial cells and novel expression of the integrins α1β1, α5β1, and αvβ3.¹⁷ Endovascular cytotrophoblasts that remodel uterine blood vessels transform their adhesion receptor phenotype to resemble that of endothelial cells, expressing vascular-endothelial cadherin, platelet-endothelial adhesion molecule-1, and vascular endothelial adhesion molecule-1.^16,18 Like endothelial cells, cytotrophoblasts express substances that influence vasculogenesis and angiogenesis, including the vascular endothelial growth factor (VEGF) family ligands VEGF-A and VEGF-C and receptors VEGFR-1 [fms-like tyrosine kinase 1 (Flt-1)] and VEGFR-3.^19–21 Expression of these molecules changes as the cells differentiate/invade, and they regulate cytotrophoblast survival in the remodeled uterine vasculature. Finally, as hemiallogeneic embryonic/fetal cells, invasive cytotrophoblasts must avoid maternal immune responses. Their expression of the nonclassical major histocompatibility complex (MHC) class I molecules HLA-G^22,23 and HLA-C, which have limited polymorphisms,^24,25 contributes to their lack of immunogenicity.Previous studies led to a rudimentary understanding of HCMV infection of the human placenta and identified several molecular mechanisms that impair functions of differentiating/invading cytotrophoblasts. HCMV infection dysregulates the expression of key integrins required for cell invasiveness,^26,27 reduces the expression of matrix metalloproteinase-9,²⁷ and down-regulates cell-cell and cell-matrix adhesion molecules,²⁸ including those required for pseudovasculogenesis¹⁶ and vascular remodeling.¹⁸ The immunosuppressive viral cytokine cmv IL-10 further reduces cytotrophoblast invasion through paracrine effects that increase IL-10 expression.^27,28 Peroxisome proliferator-activated receptor γ activation by infection also compromises cytotrophoblast functions.^29,30 In chorionic villi, the neonatal Fc receptor for IgG, expressed in syncytiotrophoblasts that contact maternal blood, transcytoses circulating maternal antibodies.^31–33 In conjunction with neutralizing titers, developmental expression of HCMV receptors, EGFR, and integrins^34–37 determines susceptibility to infection.^33,38–40 HCMV infects spatially distinct populations of cytotrophoblasts that express α1β1 and αvβ3 integrins used as surface receptors.⁴¹How HCMV disseminates to the placenta and the early stages of pathogenesis in pregnancy are still unresolved because of the virus'' extreme host range restriction. A successful approach to overcome the obstacle to studies of HCMV in vivo has been to infect SCID mice (ie, mice with severe combined immunodeficiency) that have received xenografts of human tissues. Infection of human fetal thymus/liver under the mouse kidney capsule showed that medullary epithelial cells are prominent targets of HCMV replication.⁴² Thus, dramatic interstrain differences were evident in replication of low-passage clinical isolates and laboratory strains in thymus/liver xenografts in vivo.^42,43 The strain Toledo replicates to high titers in implants, whereas the laboratory strains AD169 and Towne, serially passaged in fibroblasts, are attenuated and fail to propagate in tissues in vivo.⁴³ AD169 lacks a 15-kb segment of viral genome that encodes at least 19 open reading frames present in the genomes of all pathogenic clinical strains.⁴⁴ A deletion mutant of Toledo lacking these sequences, although exhibiting only a minor growth defect in fibroblasts, fails to replicate in thymus/liver implants in SCID mice, evidence that genes in this region are central to infection in vivo.⁴⁵ HCMV replication in endothelial and epithelial cells correlates with determinants specified by ORFs UL128-131A,^46,47 which are highly conserved in clinical isolates⁴⁸ and which elicit neutralizing antibodies in humans.^49,50Herein, we investigated HCMV pathogenesis in infected human placental villous explants and in xenografts maintained in vivo. We used a model of human placentation to investigate the vascular effects of fetal cytotrophoblasts in human placental villi transplanted beneath the kidney capsules of SCID mice.²¹ VR1814, a clinical isolate, infected cell column cytotrophoblasts in placental explants and impaired the formation of anchoring villi in vitro. In xenografts, VR1814-infected placental cells had a severely diminished capacity to invade and form lymphatic vessels. In striking contrast, AD169 replicated poorly in villous explants. In SCID mice, AD169-infected cytotrophoblasts remodeled the resident arteries, but these were faulty. Our results show, for the first time to our knowledge, that HCMV genes dispensable for growth in culture function as determinants of pathogenesis that could contribute to vascular anomalies that originate in early placentation.     

Hemodynamics and Complications Encountered with Arteriovenous Fistulas and Grafts as Vascular Access for Hemodialysis: A Review

This review article describes the current state of affairs concerning in vivo, in vitro and in numero studies on the hemodynamics in vascular access for hemodialysis. The use and complications of autogenous and non-autogenous fistulas and catheters and access port devices are explained in the first part. The major hemodynamic complications are stenosis, initiated by intimal hyperplasia development, and thrombosis. The different in literature proposed conceivable causes of intimal hyperplasia development like surgical interventions, compliance mismatch, wall shear stress (WSS) and shear rate, vessel wall thrill and blood pressure are discussed on the basis of in vivo, in vitro and in numero studies.     

雷米普利通过调节细胞外调节激酶1/2的活性抑制肺动脉高压大鼠肺血管重构

目的探讨雷米普利抑制野百合碱（MCT）诱导的肺动脉高压（PAH）大鼠肺血管重构是否与调节细胞外调节激酶1/2（ERK1/2）活性有关。方法雄性Sprague-Dawley大鼠30只,质量280～320g,随机分为：正常对照组、PAH组、PAH＋雷米普利组。PAH组和PAH＋雷米普利组一次性颈部注射MCT60mg/kg后,PAH＋雷米普利组用雷米普利灌胃,PAH组用生理盐水灌胃。对照组颈部注射生理盐水后,用生理盐水灌胃。4周后,测定大鼠的右室收缩压（RVSP）和右心室肥厚指数（RVHI）,并用图像分析软件,测定肺小动脉管壁厚度（WT）占动脉外径（ED）的百分比（WT,%）及管壁面积（WA）占血管总面积的百分比（WA,%）。放射免疫法检测肺组织中血管紧张素Ⅱ（AngⅡ）浓度。Western免疫印迹分析肺组织中ERK1/2磷酸化水平。结果PAH组的RVSP、RVHI、WT（%）、WA（%）、肺组织AngⅡ浓度和ERK1/2磷酸化水平均显著高于正常对照组;雷米普利组RVSP、RVHI、WT（%）、WA（%）、肺组织AngⅡ浓度和ERK1/2磷酸化水平均明显低于PAH组。结论雷米普利抑制MCT诱导的肺血管重构的机制可能与降低肺组织ERK1/2磷酸化水平有关。     

64排螺旋CT检测冠状动脉粥样硬化斑块与血管重构及ACS的相关性研究

目的 探讨64排螺旋CT检测冠状动脉粥样硬化斑块的临床应用价值.方法 收集在本院行64排SCT冠状动脉成像,临床确诊为冠心病患者78例,分为急性冠脉综合征(acute coronary syndrome,ACS)和稳定性心绞痛(stable angina pectoris,SAP)两组,对检出的动脉粥样硬化斑块影像学特征进行分析,分析动脉粥样硬化斑块与血管重构及ACS之间的相关性.结果 78例患者共检测到斑块256个,其中软斑块65个,中间斑块81个,钙化斑块110个;有软斑的冠状动脉正向重构率明显高于钙化斑块的冠状动脉正向重构率,有显著统计学差异(P<0.01).ACS以软斑和中间斑块为主,SAP组以钙化为主,ACS组冠状动脉正向重构率明显高于SAP组,且均有显著统计学差异(P<0.01).结论 冠状动脉粥样硬化斑块性质与血管重构及ACS有明显相关性,64排螺旋CT检测冠状动脉粥样硬化斑块具有较高的临床价值,可作为评价冠心病危险度的一种无创检查技术.     

Trophoblast- and Vascular Smooth Muscle Cell-Derived MMP-12 Mediates Elastolysis during Uterine Spiral Artery Remodeling

During the first trimester of pregnancy, the uterine spiral arteries are remodeled, creating heavily dilated conduits that lack maternal vasomotor control but allow the placenta to meet an increasing requirement for nutrients and oxygen. To effect permanent vasodilatation, the internal elastic lamina and medial elastin fibers must be degraded. In this study, we sought to identify the elastolytic proteases involved in this process. Primary first-trimester cytotrophoblasts (CTBs) derived from the placenta exhibited intracellular and membrane-associated elastase activity; membrane-associated activity was primarily attributable to matrix metalloproteinases (MMP). Indeed, Affymetrix microarray analysis and immunocytochemistry implicated MMP-12 (macrophage metalloelastase) as a key mediator of elastolysis. Cultured human aortic smooth muscle cells (HASMCs) exhibited constitutive membrane-associated elastase activity and inducible intracellular elastase activity; these cells also expressed MMP-12 protein. Moreover, a specific inhibitor of MMP-12 significantly reduced CTB- and HASMC-mediated elastolysis in vitro, to 31.7 ± 10.9% and 23.3 ± 8.7% of control levels, respectively. MMP-12 is expressed by both interstitial and endovascular trophoblasts in the first-trimester placental bed and by vascular SMCs (VSMCs) in remodeling spiral arteries. Perfusion of isolated spiral artery segments with CTB-conditioned medium stimulated MMP-12 expression in medial VSMCs. Our data support a model in which trophoblasts and VSMCs use MMP-12 cooperatively to degrade elastin during vascular remodeling in pregnancy, with the localized release of elastin peptides and CTB-derived factors amplifying elastin catabolism.Transformation of the uterine spiral arteries during the first 20 weeks of gestation ensures that a constant supply of blood is delivered to the developing placenta, at an optimal rate of flow.^1–3 This allows the placenta to meet an increasing requirement for nutrients and oxygen and enables the developing fetus to attain its growth potential. The remodeling process leads to vessel dilatation, loss of spirality, and decreased vasoactivity, allowing a nonpulsatile low-pressure supply of blood to be delivered to placental villi at the maternofetal interface. Early alterations in arterial structure include endothelial vacuolation, hypertrophy of vascular smooth muscle cells (VSMCs), and disruption of medial smooth muscle layers, which occur in the absence of fetal-derived trophoblast and correlate with perivascular accumulation of macrophages and uterine natural killer (uNK) cells.^4,5 After colonization of the uterine decidua and myometrium by extravillous cytotrophoblast (EVT), endothelial cells and VSMCs are lost from the arterial wall and replaced by trophoblast embedded in a fibrinoid matrix. Remodeling is regulated in a spatial and temporal manner, such that the successive steps of trophoblast adherence, intravasation, fibrinoid deposition, and mural incorporation are effected without any loss in vessel integrity. A complex and highly orchestrated combination of vascular cell apoptosis, dedifferentiation, and matrix breakdown is probably required to achieve this alteration in vessel wall structure.^5–9Two distinct populations of EVT originate from anchoring placental villi and contribute to vessel transformation.^10,11 Interstitial EVT invade the uterine wall, migrating through the decidua and myometrium to adopt a perivascular position. Endovascular EVT enter the lumen of the spiral arteries and migrate as far as the first third of the myometrium, colonizing the arterial wall from within. Impaired arterial remodeling is distinguished by shallow EVT invasion, decreased numbers of EVT, and the persistence of muscular, narrow-bore arteries, and is associated with second trimester miscarriage,¹² preterm labor,¹³ pre-eclampsia,¹⁴ and fetal growth restriction.¹⁵To effect a permanent increase in vessel diameter it is crucial that elastin fibers within each artery are catabolized, eliminating their capacity for stretch and recoil. Myometrial segments of the spiral arteries possess an internal elastic lamina (IEL), and the musculo-elastic media of both decidual and myometrial arteries is rich in elastic fibers.^16,17 During pregnancy, EVT traverse the IEL during mural incorporation,¹⁸ thus it is highly likely that they possess elastase activity: indeed, first-trimester EVT synthesize and secrete the elastolytic proteases matrix metalloproteinase-2 (MMP-2), MMP-7, MMP-9, cathepsin B, and cathepsin L.^19,20 Although both uNK cells and macrophages produce enzymes capable of elastolysis,⁵ uNK cells are not abundant in myometrium,²¹ and elastin breakdown is associated with the presence of endovascular EVT¹⁷ rather than macrophages.²² Previous studies have demonstrated that the availability of nitric oxide (NO) can influence protease expression and activity,^23–26 and we have shown NO to be an important regulator of trophoblast function.^27–29 As dysregulation of NO production has been implicated in the pathogenesis of pre-eclampsia and intrauterine growth restriction (IUGR),^30–32 NO availability may regulate the process of arterial remodeling by controlling trophoblast elastolysis.Rodent models of atherosclerosis have highlighted a role for VSMC-derived cathepsins as mediators of IEL breakdown during lesion formation,³³ demonstrating that the arterial wall may be a potential source of elastases. Similarly, caspase-2, −3, and −7 derived from apoptotic VSMCs have been implicated as mediators of elastin breakdown.³⁴ Thus, during the process of spiral artery transformation, resident VSMCs may also be stimulated to produce elastase(s) in response to pregnancy hormones, trophoblast invasion, or soluble factors released by cells within the placental bed. In this study we have investigated the origin and identity of the proteases involved in mediating elastin breakdown during spiral artery remodeling.     

Reconciling PC‐MRI and CFD: An in‐vitro study

Several well‐resolved 4D Flow MRI acquisitions of an idealized rigid flow phantom featuring an aneurysm, a curved channel as well as a bifurcation were performed under pulsatile regime. The resulting hemodynamics were processed to remove MRI artifacts. Subsequently, they were compared with CFD predictions computed on the same flow domain, using an in‐house high‐order low dissipative flow solver. Results show that reaching a good agreement is not straightforward but requires proper treatments of both techniques. Several sources of discrepancies are highlighted and their impact on the final correlation evaluated. While a very poor correlation (r² = 0.63) is found in the entire domain between raw MRI and CFD data, correlation as high as r² = 0.97 is found when artifacts are removed by post‐processing the MR data and down sampling the CFD results to match the MRI spatial and temporal resolutions. This work demonstrates that, in a well‐controlled environment, both PC‐MRI and CFD might bring reliable and correlated flow quantities when a proper methodology to reduce the errors is followed.     

The Role of Matrix Metalloproteinase-2 in the Remodeling of Cell-Seeded Vascular Constructs Subjected to Cyclic Strain

Tissue engineering offers the opportunity to develop vascular substitutes that mimic the responsive nature of native arteries. A good blood vessel substitute should be able to remodel its matrix in response to mechanical stimulation, as imposed by the hemodynamic environment. We have developed a novel method of studying the influence of mechanical strain on the remodeling of cell-seeded collagen gel blood vessel analogs. We assessed the remodeling capacity by examining the effect of mechanical conditioning upon the expression of enzymes which remodel the extracellular matrix, called matrix metalloproteinases (MMPs), and upon the mechanical properties of the constructs. We found that subjecting collagen constructs to a 10% cyclic radial distention, over a course of 4 days, resulted in an overall increase in the production of MMP-2. Cyclic mechanical strain also stimulated enzymatic activation of latent MMP-2. We found that cyclic strain also significantly increased the mechanical strength and material modulus, as indicated by an increase in circumferential tensile properties of the constructs. These observations suggested that MMP-2-dependent remodeling affects the material properties of vascular tissue analogs. To further investigate this possible connection we examined the effects of dynamic conditioning in the presence of two nonspecific inhibitors of MMP activity. Interestingly, we found that nonspecific inhibition of MMP ablated the benefits of mechanical conditioning upon mechanical properties. Our observations suggest that a better understanding of the complex relation between mechanical stimulation and construct remodeling is key for the proper design of tissue-engineered blood vessel substitutes. © 2001 Biomedical Engineering Society. PAC01: 8719Rr, 8714Ee, 8717-d     

左西孟旦和米力农治疗对心力衰竭患者血管内皮因子、心室重构及心功能的影响

目的探讨并对比左西孟旦和米力农对心力衰竭患者血管内皮因子、心室重构及心功能的影响。方法将2016年6月至2018年6月医院收治的80例急性失代偿期心力衰竭患者随机分为左西孟旦组和米力农组,每组各40例。治疗前和治疗7d采用超声心动图检测心功能参数[左心室收缩末期内径(left ventricular end systolic diameter,LVESD)、左心室舒张末期内径(left ventricular end diastolic diameter,LVEDD)、左心室射血分数(left ventricular ejection fractions,LVEF)],检测血清N-末端前体脑钠肽(N-terminal pro-B-type natriuretic peptid,NT-pro BNP)、血管内皮生长因子(vascular endothelial growth factor,VEGF)、白介素6(Interleukin-6,IL-6)、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α),治疗结束后2个月行6min步行实验(6-minute walk test,6MWT),记录两组不良反应。结果左西孟旦组治疗后LVESD值低于米力农组,LVEF值高于米力农组,差异有统计学意义(P <0.05),但两组治疗后LVEDD值比较,差异无统计学意义(P>0.05);左西孟旦组治疗后NT-pro BNP水平低于米力农组,6MWT距离长于米力农组,差异有统计学意义(P<0.05);左西孟旦组治疗后VEGF水平高于米力农组,IL-6、TNF-α水平低于米力农组,差异有统计学意义(P<0. 05),两组不良反应发生率比较,差异无统计学意义(P>0. 05)。结论左西孟旦、米力农均可用于治疗心力衰竭患者心室重构,改善心功能,但短期效果而言,左西孟旦优于米力农。     

静脉桥接法治疗及预防创伤性神经瘤

目的：评价静脉桥接法治疗及预防残端创伤性神经瘤的临床疗效。方法：采用静脉桥接法治疗及预防创伤性神经瘤14例。根据患者术后疼痛缓解程度、局部有无触痛、Tinel＇s征及患者的满意程度等对术后效果做出评价。结果：14例患者术后随访时间为3个月～5a，自觉疼痛症状均得到明显缓解，无自发性疼痛，局部无触痛。结论：静脉桥接法是治疗创伤性神经瘤的有效方法。     

A Membrane Associated mCherry Fluorescent Reporter Line for Studying Vascular Remodeling and Cardiac Function During Murine Embryonic Development

The development of the cardiovascular system is a highly dynamic process dependent on multiple signaling pathways regulating proliferation, differentiation, migration, cell–cell and cell‐matrix interactions. To characterize cell and tissue dynamics during the formation of the cardiovascular system in mice, we generated a novel transgenic mouse line, Tg(Flk1::myr‐mCherry), in which endothelial cell membranes are brightly labeled with mCherry, a red fluorescent protein. Tg(Flk1::myr‐mCherry) mice are viable, fertile, and do not exhibit any developmental abnormalities. High levels of mCherry are expressed in the embryonic endothelium and endocardium, and expression is also observed in capillaries in adult animals. Targeting of the fluorescent protein to the cell membrane allows for subcellular imaging and cell tracking. By acquiring confocal time lapses of live embryos cultured on the microscope stage, we demonstrate that the newly generated transgenic model beautifully highlights the sprouting behaviors of endothelial cells during vascular plexus formation. We have also used embryos from this line to imaging the endocardium in the beating embryonic mouse heart, showing that Tg(Flk1::myr‐mCherry) mice are suitable for the characterization of cardio dynamics. Furthermore, when combined with the previously described Tg(Flk1::H2B‐EYFP) line, cell number in addition to cell architecture is revealed, making it possible to determine how individual endothelial cells contribute to the structure of the vessel. Anat Rec, 2008. © 2008 Wiley‐Liss, Inc.     

高脂饮食诱导兔自体静脉移植后动脉硬化特点

目的　探讨高脂饮食诱导兔自体静脉移植动脉硬化的结构特点 ,为静脉搭桥后再狭窄的防治提供资料。方法　兔 2 5只 ,均实施自体血管移植术 ,术后按不同的饲高脂饮食时间段分为 5组。按不同时间点取材分 5组。光、电镜观察。结果　光镜下移植段管壁逐渐增厚 ,内膜泡沫细胞逐渐增多 ,12周时内膜的全层和中膜的内层充满了大量泡沫细胞 ,细胞间质较少 ;移植后早期可见内皮表面有较多的白细胞粘附并浸润到内皮下层 ,对照侧静脉和颈总动脉偶见泡沫细胞。电镜下中膜平滑肌细胞由收缩型转变为合成型 ,移植后两周时达到高峰。对照静脉内皮细胞呈长梭形 ,无微绒毛 ;在移植后 1～ 2周 ,移植段内皮的形态呈圆形 ,椭圆形或梭形等多种形态 ,有丰富的长而密的微绒毛 ,随着时间的延长 ,移植段可见成片的 ,局灶性内皮脱落。结论　自体静脉移植后 ,对高脂诱导动脉硬化的易感性高于原位血管 ;移植段管壁增厚可能与血流动力学改变和平滑肌转型、增殖、产生基质有关